mouse skin-associated 16S microbiome Raw sequence reads

Background: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) causes toxicity by activating the arylhydrocarbon receptor (AhR). Murine genetic activation of the AhR promotes atopic dermatitis (AD), a inflammatory skin disease that frequently affects children.Objective: The goal of this study was to determine the effects of in utero and lactational exposure to TCDD on murine skin barrier development and susceptibility to developing cutaneous disease later in life.Methods: Pregnant C57BL/6J mice were gavaged with vehicle or TCDD (5 ug/ kg body weight) at embryonic day 12 epidermal barrier formation and function were studied in their offspring from postnatal day 1 (P1) through adult life.Results: TCDD-exposed pups followed to P135 were born with transitory acanthosis and did not develop symptoms of AD. Lack of atopy does not appear to be due to immunosuppression as the adult control and TCDD-exposed mice reacted similarly to MC903, but may be due to the transient activation of the AhR as demonstrated by reversible increases in the AhR biomarkers, CYP1A1 and CYP1B1, and ARTN, a gene critical to atopy. Sebaceous gland hypoplasia and cyst formation, similar to chloracne, were observed in TCDD-exposed P21 mice and were reversed by P35. CYP1A1 and CYP1B1 expression co-localized with leucine-rich repeats and immunoglobulin-like domains protein 1 (LRIG1)-expressing progenitor cells at the infundibulum. Inducible CYP1B1 protein also co-localized with a second stem cell niche in the isthmus. Similar to other skin effects, skin microbiome dysbiosis occurred in TCDD-exposed mice at P21.